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3.

Adverse Health Effects Of Noise


3.1. Introduction
The perception of sounds in day-to-day life is of major importance for human well-being.
Communication through speech, sounds from playing children, music, natural sounds in
parklands, parks and gardens are all examples of sounds essential for satisfaction in every day
life. Conversely, this document is related to the adverse effects of sound (noise). According to
the International Programme on Chemical Safety (WHO 1994), an adverse effect of noise is
defined as a change in the morphology and physiology of an organism that results in impairment
of functional capacity, or an impairment of capacity to compensate for additional stress, or
increases the susceptibility of an organism to the harmful effects of other environmental
influences. This definition includes any temporary or long-term lowering of the physical,
psychological or social functioning of humans or human organs. The health significance of
noise pollution is given in this chapter under separate headings, according to the specific effects:
noise-induced hearing impairment; interference with speech communication; disturbance of rest
and sleep; psychophysiological, mental-health and performance effects; effects on residential
behaviour and annoyance; as well as interference with intended activities. This chapter also
considers vulnerable groups and the combined effects of sounds from different sources.
Conclusions based on the details given in this chapter are given in Chapter 4 as they relate to
guideline values.

3.2. Noise-Induced Hearing Impairment


Hearing impairment is typically defined as an increase in the threshold of hearing. It is assessed
by threshold audiometry. Hearing handicap is the disadvantage imposed by hearing impairment
sufficient to affect ones personal efficiency in the activities of daily living. It is usually
expressed in terms of understanding conventional speech in common levels of background noise
(ISO 1990). Worldwide, noise-induced hearing impairment is the most prevalent irreversible
occupational hazard. In the developing countries, not only occupational noise, but also
environmental noise is an increasing risk factor for hearing impairment. In 1995, at the World
Health Assembly, it was estimated that there are 120 million persons with disabling hearing
difficulties worldwide (Smith 1998). It has been shown that men and women are equally at risk
of noise-induced hearing impairment (ISO 1990; Berglund & Lindvall 1995).
Apart from noise-induced hearing impairment, hearing damage in populations is also caused by
certain diseases; some industrial chemicals; ototoxic drugs; blows to the head; accidents; and
hereditary origins. Deterioration of hearing capability is also associated with the aging process
per se (presbyacusis). Present knowledge of the physiological effects of noise on the auditory
system is based primarily on laboratory studies on animals. After noise exposure, the first
morphological changes are usually found in the inner and outer hair cells of the cochlea, where
the stereocilia become fused and bent. After more prolonged exposure, the outer and inner hair
cells related to transmission of high-frequency sounds are missing. See Berglund & Lindvall
(1995) for further discussion.
The ISO Standard 1999 (ISO 1990) gives a method for calculating noise-induced hearing
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impairment in populations exposed to all types of noise (continuous, intermittent, impulse)


during working hours. Noise exposure is characterized by LAeq over 8 hours (LAeq,8h). In the
Standard, the relationships between LAeq,8h and noise-induced hearing impairment are given
for frequencies of 5006 000 Hz, and for exposure times of up to 40 years. These relations show
that noise-induced hearing impairment occurs predominantly in the high-frequency range of 3
0006 000 Hz, the effect being largest at 4 000 Hz. With increasing LAeq,8h and increasing
exposure time, noise-induced hearing impairment also occurs at 2 000 Hz. But at LAeq,8h levels
of 75 dBA and lower, even prolonged occupational noise exposure will not result in noiseinduced hearing impairment (ISO 1990). This value is equal to that specified in 1980 by the
World Health Organization (WHO 1980a).
The ISO Standard 1999 (ISO 1990) specifies hearing impairment in statistical terms (median
values, and percentile fractions between 0.05 and 0.95). The extent of noise-induced hearing
impairment in populations exposed to occupational noise depends on the value of LAeq,8h and
the number of years of noise exposure. However, for high LAeq,8h values, individual
susceptibility seems to have a considerable effect on the rate of progression of hearing
impairment. For daily exposures of 816 h, noise-induced hearing impairment can be reasonably
well estimated from LAeq,8h extrapolated to the longer exposure times (Axelsson et al. 1986).
In this adaptation of LAeq,8h for daily exposures other than 8 hours, the equal energy principle
is assumed to be applicable. For example, the hearing impairment due to a 16 h daily exposure is
equivalent to that at LAeq,8h plus 3 dB (LAeq,16h = LAeq,8h + 10*log10 (16/8) = LAeq,8h + 3
dB. For a 24 h exposure, LAeq,24h = LAeq,8h + 10*log10 (24/8) = LAeq,8h + 5 dB).
Since the calculation method specified in the ISO Standard 1999 (ISO 1990) is the only
universally adopted method for estimating occupational noise-induced hearing impairment,
attempts have been made to assess whether the method is also applicable to hearing impairment
due to environmental noise, including leisure-time noise. There is ample evidence that shooting
noise, with LAeq,24h values of up to 80 dB, induces the same hearing impairment as an
equivalent occupational noise exposure (Smoorenburg 1998). Moreover, noise-induced hearing
impairment studies from motorbikes are also in agreement with results from ISO Standard 1999
(ISO 1990). Hearing impairment in young adults and children 12 years and older has been
assessed by LAeq on a 24 h time basis, for a variety of environmental and leisure-time exposure
patterns (e.g. Passchier-Vermeer 1993; HCN 1994). These include pop music in discotheques
and concerts (Babisch & Ising 1989; ISO 1990); pop music through headphones (Ising et al.
1994; Struwe et al. 1996; Passchier-Vermeer et al. 1998); music played by brass bands and
symphony orchestras (van Hees 1992). The results are in agreement with values predicted by the
ISO Standard 1999 method on the basis of adjusted time.
In the publications cited above, exposure to noise with known characteristics, such as duration
and level, was related to hearing impairment. In addition to these publications, there is also an
extensive literature showing hearing impairment in populations exposed to specific types of nonoccupational noise, although these exposures are not well characterized. These noises originate
from shooting, motorcycling, snowmobile driving, playing in arcades, listening to music at
concerts and through headphones, using noisy toys, and fireworks (e.g. Brookhouser et al. 1992;
see also Berglund & Lindvall 1995). Although the characteristics of these exposures are to a
certain extent unknown, the details in the publications suggest that LAeq,24h values of these

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exposures exceed 70 dB.


In contrast, epidemiological studies failed to show hearing damage in populations exposed to an
LAeq,24h of less than 70 dB (Lindemann et al. 1987). The data imply that even a lifetime
exposure to environmental and leisure-time noise with an LAeq,24h <70 dBA would not cause
hearing impairment in the large majority of people (over 95%). Overall, the results of many
studies strongly suggest that the method from ISO Standard 1999 can also be used to estimate
hearing impairment due to environmental and leisure-time noise, in addition to estimating the
effects of occupational noise exposure.
Although the evidence suggests that the calculation method from ISO Standard 1999 (ISO 1990)
should also be accepted for environmental and leisure time noise exposures, large-scale
epidemiological studies of the general population do not exist to support this proposition.
Taking into account the limitations of the studies, care should be taken with respect to the
following aspects:
a. Data from animal experiments indicate that children may be more vulnerable in
acquiring noise-induced hearing impairment than adults.
b. At very high instantaneous sound pressure levels, mechanical damage to the ear may
occur (Hanner & Axelsson 1988). Occupational limits are set at peak sound pressure
levels of 140 dB (EU 1986a). For adults exposed to environmental and leisure-time
noise, this same limit is assumed to be valid. In the case of children, however, taking
into account their habits while playing with noisy toys, peak sound pressure levels
should never exceed 120 dB.
c. For shooting noise with LAeq,24h over 80 dB, studies on temporary threshold shift
suggest the possibility of an increased risk for noise-induced hearing impairment
(Smoorenburg 1998).
d. Risk for noise-induced hearing impairment may increase when the noise exposure is
combined with exposure to vibrations, the use of ototoxic drugs, or some chemicals
(Fechter 1999). In these circumstances, long-term exposure to LAeq,24h of 70 dBA
may induce small hearing impairments.
e. It is uncertain whether the relationships between hearing impairment and noise
exposure given in ISO Standard 1999 (ISO 1990) are applicable for environmental
sounds of short rise time. For example, in the case of military low-altitude flying
areas (75300 m above ground) LAmax values of 110130 dB occur within seconds
after the onset of the sound.
Usually noise-induced hearing impairment is accompanied by an abnormal loudness perception
which is known as loudness recruitment (cf. Berglund & Lindvall 1995). With a considerable
loss of auditory sensitivity, some sounds may be perceived as distorted (paracusis). Another
sensory effect that results from noise exposure is tinnitus (ringing in the ears). Commonly,
tinnitus is referred to as sounds that are emitted by the inner ear itself (physiological tinnitus).

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Tinnitus is a common and often disturbing accompaniment of occupational hearing impairment


(Vernon and Moller 1995) and has become a risk for teenagers attending pop concerts and
discotheques (Hetu & Fortin 1995; Passchier-Vermeer et al. 1998; Axelsson & Prasher 1999).
Noise-induced tinnitus may be temporary, lasting up to 24 hours after exposure, or may have a
more permanent character, such as after prolonged occupational noise exposure. Sometimes
tinnitus is due to the sound produced by the blood flow through structures in the ear.
The main social consequence of hearing impairment is an inability to understand speech in daily
living conditions, which is considered a severe social handicap. Even small values of hearing
impairment (10 dB averaged over 2 000 and 4 000 Hz, and over both ears) may have an effect on
the understanding of speech. When the hearing impairment exceeds 30 dB (again averaged over
2 000 and 4 000 Hz and both ears) a social hearing handicap is noticeable (cf. Katz 1994;
Berglund & Lindvall 1995).
In the past, hearing protection has mainly emphasized occupational noise exposures at high
values of LAeq,8h, or situations with high impulsive sounds. The near-universal adoption of an
LAeq,8h value of 85 dB (or lower) as the limit for unprotected occupational noise exposure,
together with requirements for personal hearing protection, has made cases of severe unprotected
exposures more rare. This is particularly true for developed countries. However, monitoring of
compliance and enforcement action for sound pressure levels just over the limits may be weak,
especially in non-industrial environments in developed countries (Franks 1998), as well as in
occupational and urban environments in developing countries (Smith 1998). Nevertheless,
regulations for occupational noise exposure exist almost worldwide and exposures to
occupational noise are to a certain extent under control.
On the other hand, environmental noise exposures due to a number of noisy activities, especially
those during leisure-time activities of children and young adults, have scarcely been regulated.
Given both the increasing number of noisy activities and the increasing exposure duration, such
as loud music in cars and the use of Walkmen and Discmen, regulatory activities in this field are
to be encouraged. Dose-response data are lacking for the general population. However, judging
from the limited data for study groups (teenagers, young adults and women), and the assumption
that time of exposure can be equated with sound energy, the risk for hearing impairment would
be negligible for LAeq,24h values of 70 dBA over a lifetime. To avoid hearing impairment,
impulse noise exposures should never exceed 140 dB peak sound pressure in adults, and 120 dB
peak sound pressure in children.

3.3. Interference with Speech Communication


Noise interference with speech comprehension results in a large number of personal disabilities,
handicaps and behavioural changes. Problems with concentration, fatigue, uncertainty and lack
of self-confidence, irritation, misunderstandings, decreased working capacity, problems in
human relations, and a number of stress reactions have all been identified (Lazarus 1998).
Particularly vulnerable to these types of effects are the hearing impaired, the elderly, children in
the process of language and reading acquisition, and individuals who are not familiar with the
spoken language (e.g., Lazarus 1998). Thus, vulnerable persons constitute a substantial
proportion of a countrys population.

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Most of the acoustical energy of speech is in the frequency range 1006 000 Hz, with the most
important cue-bearing energy being between 3003 000 Hz. Speech interference is basically a
masking process in which simultaneous, interfering noise renders speech incapable of being
understood. The higher the level of the masking noise, and the more energy it contains at the
most important speech frequencies, the greater will be the percentage of speech sounds that
become indiscernible to the listener. Environmental noise may also mask many other acoustical
signals important for daily life, such as door bells, telephone signals, alarm clocks, fire alarms
and other warning signals, and music (e.g., Edworthy & Adams 1996). The masking effect of
interfering noise in speech discrimination is more pronounced for hearing-impaired persons than
for persons with normal hearing, particularly if the interfering noise is composed of speech or
babble.
As the sound pressure level of an interfering noise increases, people automatically raise their
voice to overcome the masking effect upon speech (increase of vocal effort). This imposes an
additional strain on the speaker. For example, in quiet surroundings, the speech level at 1 m
distance averages 4550 dBA, but is 30 dBA higher when shouting. However, even if the
interfering noise is moderately loud, most of the sentences during ordinary conversation can still
be understood fairly well. Nevertheless, the interpretation required for compensating the
masking effect of the interfering sounds, and for comprehending what was said, imposes an
additional strain on the listener. One contributing factor could be that speech spoken loudly is
more difficult to understand than speech spoken softly, when compared at a constant speech-tonoise ratio (cf. Berglund & Lindvall 1995).
Speech levels vary between individuals because of factors such as gender and vocal effort.
Moreover, outdoor speech levels decrease by about 6 dB for a doubling in the distance between
talker and listener. Speech intelligibility in everyday living conditions is influenced by speech
level, speech pronunciation, talker-to-listener distance, sound pressure levels, and to some extent
other characteristics of interfering noise, as well as room characteristics (e.g. reverberation).
Individual capabilities of the listener, such as hearing acuity and the level of attention of the
listener, are also important for the intelligibility of speech. Speech communication is affected
also by the reverberation characteristics of the room. For example, reverberation times greater
than 1 s produce loss in speech discrimination. Longer reverberation times, especially when
combined with high background interfering noise, make speech perception more difficult. Even
in a quiet environment, a reverberation time below 0.6 s is desirable for adequate speech
intelligibility by vulnerable groups. For example, for older hearing-handicapped persons, the
optimal reverberation time for speech intelligibility is 0.30.5 s (Plomp 1986).
For complete sentence intelligibility in listeners with normal hearing, the signal-to-noise ratio
(i.e. the difference between the speech level and the sound pressure level of the interfering noise)
should be 1518 dBA (Lazarus 1990). This implies that in smaller rooms, noise levels above 35
dBA interferes with the intelligibility of speech (Bradley 1985). Earlier recommendations
suggested that sound pressure levels as high as 45 dBA would be acceptable (US EPA 1974).
With raised voice (increased vocal effort) sentences may be 100% intelligible for noise levels of
up to 55 dBA; and sentences spoken with straining vocal effort can be 100% intelligible with
noise levels of about 65 dBA. For speech to be intelligible when listening to complicated

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messages (at school, listening to foreign languages, telephone conversation), it is recommended


that the signal-to-noise ratio should be at least 15 dBA. Thus, with a speech level of 50 dBA, (at
1 m distance this level corresponds to a casual speech level of both women and men), the sound
pressure level of interfering noise should not exceed 35 dBA. For vulnerable groups even lower
background levels are needed. If it is not possible to meet the strictest criteria for vulnerable
persons in sensitive situations (e.g. in classrooms), one should strive for as low background
levels as possible.

3.4. Sleep Disturbance


Uninterrupted sleep is known to be a prerequisite for good physiological and mental functioning
of healthy persons (Hobson 1989); sleep disturbance, on the other hand, is considered to be a
major environmental noise effect. It is estimated that 80-90% of the reported cases of sleep
disturbance in noisy environments are for reasons other than noise originating outdoors. For
example, sanitary needs; indoor noises from other occupants; worries; illness; and climate (e.g.
Reyner & Horne 1995). Our understanding of the impact of noise exposure on sleep stems
mainly from experimental research in controlled environments. Field studies conducted with
people in their normal living situations are scarce. Most of the more recent field research on
sleep disturbance has been conducted for aircraft noise (Fidell et al. 1994 1995a,b 1998; Horne et
al. 1994 1995; Maschke et al. 1995 1996; Ollerhead et al. 1992; Passchier-Vermeer 1999). Other
field studies have examined the effects of road traffic and railway noise (Griefahn et al. 1996
1998).
The primary sleep disturbance effects are: difficulty in falling asleep (increased sleep latency
time); awakenings; and alterations of sleep stages or depth, especially a reduction in the
proportion of REM-sleep (REM = rapid eye movement) (Hobson 1989). Other primary
physiological effects can also be induced by noise during sleep, including increased blood
pressure; increased heart rate; increased finger pulse amplitude; vasoconstriction; changes in
respiration; cardiac arrhythmia; and an increase in body movements (cf. Berglund & Lindvall
1995). For each of these physiological effects, both the noise threshold and the noise-response
relationships may be different. Different noises may also have different information content and
this also could affect physiological threshold and noise-response relationships (Edworthy 1998).
Exposure to night-time noise also induces secondary effects, or so-called after effects. These are
effects that can be measured the day following the night-time exposure, while the individual is
awake. The secondary effects include reduced perceived sleep quality; increased fatigue;
depressed mood or well-being; and decreased performance (hrstrm 1993a; Passchier-Vermeer
1993; Carter 1996; Pearsons et al. 1995; Pearsons 1998).
Long-term effects on psychosocial well-being have also been related to noise exposure during
the night (hrstrm 1991). Noise annoyance during the night-time increased the total noise
annoyance expressed by people in the following 24 h. Various studies have also shown that
people living in areas exposed to night-time noise have an increased use of sedatives or sleeping
pills. Other frequently reported behavioural effects of night-time noise include closed bedroom
windows and use of personal hearing protection. Sensitive groups include the elderly, shift
workers, persons especially vulnerable to physical or mental disorders and other individuals with

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sleeping difficulties.
Questionnaire data indicate the importance of night-time noise on the perception of sleep quality.
A recent Japanese investigation was conducted for 3 600 women (2080 years old) living in
eight roadside zones with different road traffic noise. The results showed that four measures of
perceived sleep quality (difficulty in falling asleep; waking up during sleep; waking up too early;
feelings of sleeplessness one or more days a week) correlated significantly with the average
traffic volumes during night-time. An in-depth investigation of 19 insomnia cases and their
matched controls (age,work) measured outdoor and indoor sound pressure levels during sleep
(Kageyama et al. 1997). The study showed that road traffic noise in excess of 30 dB LAeq for
nighttime induced sleep disturbance, consistent with the results of hrstrm (1993b).
Meta-analyses of field and laboratory studies have suggested that there is a relationship between
the SEL for a single night-time noise event and the percentage of people awakened, or who
showed sleep stage changes (e.g. Ollerhead et al. 1992; Passchier-Vermeer 1993; Finegold et al.
1994; Pearsons et al. 1995). All of these studies assumed that the number of awakenings per
night for each SEL value is proportional to the number of night-time noise events. However, the
results have been criticized for methodological reasons. For example, there were small groups of
sleepers; too few original studies; and indoor exposure was estimated from outdoor sound
pressure levels (NRC-CNRC 1994; Beersma & Altena 1995; Vallet 1998). The most important
result of the meta-analyses is that there is a clear difference in the dose-response curves for
laboratory and field studies, and that noise has a lower effect under real-life conditions (Pearsons
et al. 1995; Pearsons 1998).
However, this result has been questioned, because the studies were not controlled for such things
as the sound insulation of the buildings, and the number of bedrooms with closed windows.
Also, only two indicators of sleep disturbance were considered (awakening and sleep stage
changes). The meta-analyses thus neglected other important sleep disturbance effects (hrstrm
1993b; Carter et al. 1994a; Carter et al. 1994b; Carter 1996; Kuwano et al. 1998). For example,
for road traffic noise, perceived sleep quality is related both to the time needed to fall asleep and
the total sleep time (hrstrm & Bjrkman 1988). Individuals who are more sensitive to noise
(as assessed by different questionnaires) report worse sleep quality both in field studies and in
laboratory studies.
A further criticism of the meta-analyses is that laboratory experiments have shown that
habituation to night-time noise events occurs, and that noise-induced awakening decreases with
increasing number of sound exposures per night. This is in contrast to the assumption used in the
meta-analyses, that the percentage of awakenings is linearly proportional to the number of nighttime noise events. Studies have also shown that the frequency of noise-induced awakenings
decreases for at least the first eight consecutive nights. So far, habituation has been shown for
awakenings, but not for heart rate and after effects such as perceived sleep quality, mood and
performance (hrstrm and Bjrkman 1988).
Other studies suggest that it is the difference in sound pressure levels between a noise event and
background, rather than the absolute sound pressure level of the noise event, that determines the
reaction probability. The time interval between two noise events also has an important influence

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of the probability of obtaining a response (Griefahn 1977; cf. Berglund & Lindvall 1995).
Another possible factor is the persons age, with older persons having an increased probability of
awakening. However, one field study showed that noise-induced awakenings are independent of
age (Reyner & Horne 1995).
For a good sleep, it is believed that indoor sound pressure levels should not exceed
approximately 45 dB LAmax more than 1015 times per night (Vallet & Vernet 1991), and most
studies show an increase in the percentage of awakenings at SEL values of 5560 dBA
(Passchier-Vermeer 1993; Finegold et al. 1994; Pearsons et al. 1995). For intermittent events
that approximate aircraft noise, with an effective duration of 1030 s, SEL values of 5560 dBA
correspond to a LAmax value of 45 dB. Ten to 15 of these events during an eight-hour nighttime implies an LAeq,8h of 2025 dB. This is 510 dB below the LAeq,8h of 30 dB for
continuous night-time noise exposure, and shows that the intermittent character of noise has to
be taken into account when setting night-time limits for noise exposure. For example, this can be
achieved by considering the number of noise events and the difference between the maximum
sound pressure level and the background level of these events.
Special attention should also be given to the following considerations:
a. Noise sources in an environment with a low background noise level. For example,
night-traffic in suburban residential areas.
b. Environments where a combination of noise and vibrations are produced.
example, railway noise, heavy duty vehicles.

For

c. Sources with low-frequency components. Disturbances may occur even though the
sound pressure level during exposure is below 30 dBA.
If negative effects on sleep are to be avoided the equivalent sound pressure level should not
exceed 30 dBA indoors for continuous noise. If the noise is not continuous, sleep disturbance
correlates best with LAmax and effects have been observed at 45 dB or less. This is particularly
true if the background level is low. Noise events exceeding 45 dBA should therefore be limited
if possible. For sensitive people an even lower limit would be preferred. It should be noted that
it should be possible to sleep with a bedroom window slightly open (a reduction from outside to
inside of 15 dB). To prevent sleep disturbances, one should thus consider the equivalent sound
pressure level and the number and level of sound events. Mitigation targeted to the first part of
the night is believed to be effective for the ability to fall asleep.

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3.5. Cardiovascular and Physiological Effects


Epidemiological and laboratory studies involving workers exposed to occupational noise, and
general populations (including children) living in noisy areas around airports, industries and
noisy streets, indicate that noise may have both temporary and permanent impacts on
physiological functions in humans. It has been postulated that noise acts as an environmental
stressor (for a review see Passchier-Vermeer 1993; Berglund & Lindvall 1995). Acute noise
exposures activate the autonomic and hormonal systems, leading to temporary changes such as
increased blood pressure, increased heart rate and vasoconstriction. After prolonged exposure,
susceptible individuals in the general population may develop permanent effects, such as
hypertension and ischaemic heart disease associated with exposures to high sound pressure levels
(for a review see Passchier-Vermeer 1993; Berglund & Lindvall 1995). The magnitude and
duration of the effects are determined in part by individual characteristics, lifestyle behaviours
and environmental conditions. Sounds also evoke reflex responses, particularly when they are
unfamiliar and have a sudden onset.
Laboratory experiments and field quasi-experiments show that if noise exposure is temporary,
the physiological system usually returns - after the exposure terminates - to a normal (preexposure) state within a time in the range of the exposure duration. If the exposure is of
sufficient intensity and unpredictability, cardiovascular and hormonal responses may appear,
including increases in heart rate and peripheral vascular resistance; changes in blood pressure,
blood viscosity and blood lipids; and shifts in electrolyte balance (Mg/Ca) and hormonal levels
(epinephrine, norepinephrine, cortisol). The first four effects are of interest because of noiserelated coronary heart disease (Ising & Gnther 1997). Laboratory and clinical data suggest that
noise may significantly elevate gastrointestinal motility in humans.
By far the greatest number of occupational and community noise studies have focused on the
possibility that noise may be a risk factor for cardiovascular disease. Many studies in
occupational settings have indicated that workers exposed to high levels of industrial noise for 5
30 years have increased blood pressure and statistically significant increases in risk for
hypertension, compared to workers in control areas (Passchier-Vermeer 1993). In contrast, only
a few studies on environmental noise have shown that populations living in noisy areas around
airports and on noisy streets have an increased risk for hypertension. The overall evidence
suggests a weak association between long-term environmental noise exposure and hypertension
(HCN 1994; Berglund & Lindvall 1995; IEH 1997), and no dose-response relationships could be
established.
Recently, an updated summary of available studies for ischaemic heart disease has been
presented (Babisch 1998a; Babisch 1998b; Babisch et al. 1999; see also Thompson 1996). The
studies reviewed include case-control and cross-sectional designs, as well as three longitudinal
studies. However, it has not yet been possible to conduct the most advanced quantitative
integrated analysis of the available studies. Relative risks and their confidence intervals could be
estimated only for the classes of high noise levels (mostly >65 dBA during daytime) and low
levels (mostly <55 dBA during daytime), rather than a range of exposure levels. For
methodological reasons identified in the meta-analysis, a cautious interpretation of the results is
warranted (Lercher et al. 1998).

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Prospective studies that controlled for confounding factors suggest an increase in ischaemic heart
disease when the noise levels exceed 6570 dB for LAeq (622). (For road traffic noise, the
difference between LAeq (6-22h) and LAeq,24h usually is of the order of 1.5 dB). When
orientation of the bedroom, window opening habits and years of exposure are taken into account,
the risk of heart disease is slightly higher (Babisch et al. 1998; Babisch et al. 1999). However,
disposition, behavioural and environmental factors were not sufficiently accounted for in the
analyses carried out to date. In epidemiological studies the lowest level at which traffic noise
had an effect on ischaemic heart disease was 70 dB for LAeq,24h (HCN 1994).
The overall conclusion is that cardiovascular effects are associated with long-term exposure to
LAeq,24h values in the range of 6570 dB or more, for both air- and road-traffic noise.
However, the associations are weak and the effect is somewhat stronger for ischaemic heart
disease than for hypertension. Nevertheless, such small risks are potentially important because a
large number of persons are currently exposed to these noise levels, or are likely to be exposed in
the future. Furthermore, only the average risk is considered and sensitive subgroups of the
populations have not been sufficiently characterized. For example, a 10% increase in risk factors
(a relative risk of 1.1) may imply an increase of up to 200 cases per 100 000 people at risk per
year. Other observed psychophysiological effects, such as changes in stress hormones,
magnesium levels, immunological indicators, and gastrointestinal disturbances are too
inconsistent for conclusions to be drawn about the influence of noise pollution.

3.6. Mental Health Effects


Mental health is defined as the absence of identifiable psychiatric disorders according to current
norms (Freeman 1984). Environmental noise is not believed to be a direct cause of mental
illness, but it is assumed that it accelerates and intensifies the development of latent mental
disorder. Studies on the adverse effects of environmental noise on mental health cover a variety
of symptoms, including anxiety; emotional stress; nervous complaints; nausea; headaches;
instability; argumentativeness; sexual impotency; changes in mood; increase in social conflicts,
as well as general psychiatric disorders such as neurosis, psychosis and hysteria. Large-scale
population studies have suggested associations between noise exposure and a variety of mental
health indicators, such as single rating of well-being; standard psychological symptom profiles;
the intake of psychotropic drugs; and consumption of tranquilizers and sleeping pills. Early
studies showed a weak association between exposure to aircraft noise and psychiatric hospital
admissions in the general population surrounding an airport (see also Berglund & Lindvall
1995). However, the studies have been criticized because of problems in selecting variables and
in response bias (Halpern 1995).
Exposure to high levels of occupational noise has been associated with development of neurosis
and irritability; and exposure to high levels of environmental noise with deteriorated mental
health (Stansfeld 1992). However, the findings on environmental noise and mental health effects
are inconclusive (HCN 1994; Berglund & Lindvall 1995; IEH 1997). The only longitudinal
study in this field (Stansfeld et al. 1996) showed an association between the initial level of road
traffic noise and minor psychiatric disorders, although the association for increased anxiety was
weak and non-linear. It turned out that psychiatric disorders are associated with noise sensitivity,

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rather than with noise exposure, and the association was found to disappear after adjustment for
baseline trait anxiety. These and other results show the importance of taking vulnerable groups
into account, because they may not be able to cope sufficiently with unwanted environmental
noise (e.g. Stansfeld 1992). This is particularly true of children, the elderly and people with
preexisting illnesses, especially depression (IEH 1997). Despite the weaknesses of the various
studies, the possibility that community noise has adverse effects on mental health is suggested by
studies on the use of medical drugs, such as tranquilizers and sleeping pills, on psychiatric
symptoms and on mental hospital admission rates.

3.7. The Effects of Noise on Performance


It has been documented in both laboratory subjects and in workers exposed to occupational
noise, that noise adversely affects cognitive task performance. In children, too, environmental
noise impairs a number of cognitive and motivational parameters (Cohen et al. 1980; Evans &
Lepore 1993; Evans 1998; Hygge et al. 1998; Haines et al. 1998). However, there are no
published studies on whether environmental noise at home also impairs cognitive performance in
adults. Accidents may also be an indicator of performance deficits. The few field studies on the
effects of noise on performance and safety showed that noise may produce some task impairment
and increase the number of errors in work, but the effects depend on the type of noise and the
task being performed (Smith 1990).
Laboratory and workplace studies showed that noise can act as a distracting stimulus. Also,
impulsive noise events (e.g. sonic booms) may produce disruptive effects as a result of startle
responses. In the short term, noise-induced arousal may produce better performance of simple
tasks, but cognitive performance deteriorates substantially for more complex tasks (i.e. tasks that
require sustained attention to details or to multiple cues; or tasks that demand a large capacity of
working memory, such as complex analytical processes). Some of the effects are related to loss
in auditory comprehension and language acquisition, but others are not (Evans & Maxwell
1997). Among the cognitive effects, reading, attention, problem solving and memory are most
strongly affected by noise. The observed effects on motivation, as measured by persistence with
a difficult cognitive task, may either be independent or secondary to the aforementioned
cognitive impairments.
Two types of memory deficits have been identified under experimental noise exposure:
incidental memory and memory for materials that the observer was not explicitly instructed to
focus on during a learning phase. For example, when presenting semantic information to
subjects in the presence of noise, recall of the information content was unaffected, but the
subjects were significantly less able to recall, for example, in which corner of the slide a word
had been located. There is also some evidence that the lack of helping behavior that was noted
under experimental noise exposure may be related to inattention to incidental cues (Berglund &
Lindvall 1995). Subjects appear to process information faster in working memory during noisy
performance conditions, but at a cost of available memory capacity. For example, in a running
memory task, in which subjects were required to recall in sequence letters that they had just
heard, subjects recalled recent items better under noisy conditions, but made more errors farther
back into the list.

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Experimental noise exposure consistently produces negative after-effects on performance (Glass


& Singer 1972). Following exposure to aircraft noise, schoolchildren in the vicinity of Los
Angeles airport were found to be deficient in proofreading, and in persistence with challenging
puzzles (Cohen et al. 1980). The uncontrollability of noise, rather than the intensity of the noise,
appears to be the most critical variable. The only prospective study on noise-exposed
schoolchildren, designed around the move of the Munich airport (Hygge et al. 1996; Evans et al.
1998), confirmed the results of laboratory and workplace studies in adults, as well the results of
the Los Angeles airport study with children (Cohen et al. 1980). An important finding was that
some of the adaptation strategies for dealing with aircraft noise, such as tuning out or ignoring
the noise, and the effort necessary to maintain task performance, come at a price. There is
heightened sympathetic arousal, as indicated by increased levels of stress hormone, and elevation
of resting blood pressure (Evans et al. 1995; Evans et al. 1998). Notably, in the airport studies
reported above, the adverse effects were larger in children with lower school achievement.
For aircraft noise, it has been shown that chronic exposure during early childhood appears to
impair reading acquisition and reduces motivational capabilities. Of recent concern are
concomitant psychophysiological changes (blood pressure and stress hormone levels). Evidence
indicates that the longer the exposure, the greater the damage. It seems clear that daycare centers
and schools should not be located near major sources of noise, such as highways, airports and
industrial sites.

3.8. Effects of Noise on Residential Behaviour and Annoyance


Noise annoyance is a global phenomenon. A definition of annoyance is a feeling of displeasure
associated with any agent or condition, known or believed by an individual or group to adversely
affect them (Lindvall & Radford 1973; Koelega 1987). However, apart from annoyance,
people may feel a variety of negative emotions when exposed to community noise, and may
report anger, disappointment, dissatisfaction, withdrawal, helplessness, depression, anxiety,
distraction, agitation, or exhaustion (Job 1993; Fields et al. 1997 1998). Thus, although the term
annoyance does not cover all the negative reactions, it is used for convenience in this document.
Noise can produce a number of social and behavioural effects in residents, besides annoyance
(for review see Berglund & Lindvall 1995). The social and behavioural effects are often
complex, subtle and indirect. Many of the effects are assumed to be the result of interactions
with a number of non-auditory variables. Social and behavioural effects include changes in overt
everyday behaviour patterns (e.g. closing windows, not using balconies, turning TV and radio to
louder levels, writing petitions, complaining to authorities); adverse changes in social behaviour
(e.g. aggression, unfriendliness, disengagement, non-participation); adverse changes in social
indicators (e.g. residential mobility, hospital admissions, drug consumption, accident rates); and
changes in mood (e.g. less happy, more depressed).
Although changes in social behaviour, such as a reduction in helpfulness and increased
aggressiveness, are associated with noise exposure, noise exposure alone is not believed to be
sufficient to produce aggression. However, in combination with provocation or pre-existing
anger or hostility, it may trigger aggression. It has also been suspected that people are less
willing to help, both during exposure and for a period after exposure. Fairly consistent evidence

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shows that noise above 80 dBA is associated with reduced helping behaviour and increased
aggressive behaviour. Particularly, there is concern that high-level continuous noise exposures
may contribute to the susceptibility of schoolchildren to feelings of helplessness (Evans &
Lepore 1993)
The effects of community noise can be evaluated by assessing the extent of annoyance (low,
moderate, high) among exposed individuals; or by assessing the disturbance of specific activities,
such as reading, watching television and communication. The relationship between annoyance
and activity disturbances is not necessarily direct and there are examples of situations where the
extent of annoyance is low, despite a high level of activity disturbance. For aircraft noise, the
most important effects are interference with rest, recreation and watching television. This is in
contrast to road traffic noise, where sleep disturbance is the predominant effect (Berglund &
Lindvall 1995).
A number of studies have shown that equal levels of traffic and industrial noises result in
different magnitudes of annoyance (Hall et al. 1981; Griffiths 1983; Miedema 1993; Bradley
1994a; Miedema & Vos 1998). This has led to criticism (e.g. Kryter 1994; Bradley 1994a) of
averaged dose-response curves determined by meta-analysis, which assumed that all traffic
noises are the same (Fidell et al. 1991; Fields 1994a; Finegold et al. 1994). Schultz (1978) and
Miedema & Vos (1998) have synthesized curves of annoyance associated with three types of
traffic noise (road, air, railway). In these curves, the percentage of people highly or moderately
annoyed was related to the day and night continuous equivalent sound level, Ldn . For each of the
three types of traffic noise, the percentage of highly annoyed persons in a population started to
increase at an Ldn value of 42 dBA, and the percentage of moderately annoyed persons at an Ldn
value of 37 dBA (Miedema & Vos 1998). Aircraft noise produced a stronger annoyance
response than road traffic, for the same Ldn exposure, consistent with earlier analyses (Kryter
1994; Bradley 1994a). However, caution should be exercised when interpreting synthesized data
from different studies, since five major parameters should be randomly distributed for the
analyses to be valid: personal, demographic, and lifestyle factors, as well as the duration of noise
exposure and the population experience with noise (Kryter 1994).
Annoyance in populations exposed to environmental noise varies not only with the acoustical
characteristics of the noise (source, exposure), but also with many non-acoustical factors of
social, psychological, or economic nature (Fields 1993). These factors include fear associated
with the noise source, conviction that the noise could be reduced by third parties, individual
noise sensitivity, the degree to which an individual feels able to control the noise (coping
strategies), and whether the noise originates from an important economic activity. Demographic
variables such as age, sex and socioeconomic status, are less strongly associated with annoyance.
The correlation between noise exposure and general annoyance is much higher at the group level
than at the individual level, as might be expected. Data from 42 surveys showed that at the
group level about 70% of the variance in annoyance is explained by noise exposure
characteristics, whereas at the individual level it is typically about 20% (Job 1988).
When the type and amount of noise exposure is kept constant in the meta-analyses, differences
between communities, regions and countries still exist (Fields 1990; Bradley 1996). This is well
demonstrated by a comparison of the dose-response curve determined for road-traffic noise

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(Miedema & Vos 1998) and that obtained in a survey along the North-South transportation route
through the Austrian Alps (Lercher 1998b). The differences may be explained in terms of the
influence of topography and meteorological factors on acoustical measures, as well as the low
background noise level on the mountain slopes.
Stronger reactions have been observed when noise is accompanied by vibrations and contains
low frequency components (Paulsen & Kastka 1995; hrstrm 1997; for review see Berglund et
al. 1996), or when the noise contains impulses, such as shooting noise (Buchta 1996; Vos 1996;
Smoorenburg 1998). Stronger, but temporary, reactions also occur when noise exposure is
increased over time, in comparison to situations with constant noise exposure (e.g. HCN 1997;
Klboe et al. 1998). Conversely, for road traffic noise, the introduction of noise protection
barriers in residential areas resulted in smaller reductions in annoyance than expected for a
stationary situation (Kastka et al. 1995).
To obtain an indicator for annoyance, other methods of combining parameters of noise exposure
have been extensively tested, in addition to metrics such as LAeq,24h and Ldn . When used for a
set of community noises, these indicators correlate well both among themselves and with
LAeq,24h or Ldn values (e.g. HCN 1997). Although LAeq,24h and Ldn are in most cases
acceptable approximations, there is a growing concern that all the component parameters of the
noise should be individually assessed in noise exposure investigations, at least in the complex
cases (Berglund & Lindvall 1995).

3.9. The Effects of Combined Noise Sources


Many acoustical environments consist of sounds from more than one source. For these
environments, health effects are associated with the total noise exposure, rather than with the
noise from a single source (WHO 1980b). When considering hearing impairment, for example,
the total noise exposure can be expressed in terms of LAeq,24h for the combined sources. For
other adverse health effects, however, such a simple model most likely will not apply. It is
possible that some disturbances (e.g. speech interference, sleep disturbance) may more easily be
attributed to specific noises. In cases where one noise source clearly dominates, the magnitude
of an effect may be assessed by taking into account the dominant source only (HCN 1997).
Furthermore, at a policy level, there may be little need to identify the adverse effect of each
specific noise, unless the responsibility for these effects is to be shared among several polluters
(cf. The Polluter Pays Principle in Chapter 5, UNCED 1992).
There is no consensus on a model for assessing the total annoyance due to a combination of
environmental noise sources. This is partly due to a lack of research into the temporal patterns of
combined noises. The current approach for assessing the effects of mixed noise sources is
limited to data on total annoyance transformed to mathematical principles or rules of thumb
(Ronnebaum et al. 1996; Vos 1992; Miedema 1996; Berglund & Nilsson 1997). Models to
assess the total annoyance of combinations of environmental noises may not be applicable to
those health effects for which the mechanisms of noise interaction are unknown, and for which
different cumulative or synergistic effects cannot be ruled out. When noise is combined with
different types of environmental agents, such as vibrations, ototoxic chemicals, or chemical
odours, again there is insufficient knowledge to accurately assess the combined effects on health

52

(Berglund & Lindvall 1995; HCN 1994; Miedema 1996; Zeichart 1998; Passchier-Vermeer &
Zeichart 1998). Therefore, caution should be exercised when trying to predict the adverse health
effects of combined factors in residential populations.
The evidence on low-frequency noise is sufficiently strong to warrant immediate concern.
Various industrial sources emit continuous low-frequency noise (compressors, pumps, diesel
engines, fans, public works); and large aircraft, heavy-duty vehicles and railway traffic produce
intermittent low-frequency noise. Low-frequency noise may also produce vibrations and rattles
as secondary effects. Health effects due to low-frequency components in noise are estimated to
be more severe than for community noises in general (Berglund et al. 1996). Since A-weighting
underestimates the sound pressure level of noise with low-frequency components, a better
assessment of health effects would be to use C-weighting.
In residential populations heavy noise pollution will most certainly be associated with a
combination of health effects. For example, cardiovascular disease, annoyance, speech
interference at work and at home, and sleep disturbance. Therefore, it is important that the total
adverse health load over 24 hours be considered and that the precautionary principle for
sustainable development is applied in the management of health effects (see Chapter 5).

3.10.

Vulnerable Groups

Protective standards are essentially derived from observations on the health effects of noise on
normal or average populations. The participants of these investigations are selected from the
general population and are usually adults. Sometimes, samples of participants are selected
because of their easy availability. However, vulnerable groups of people are typically
underrepresented. This group includes people with decreased personal abilities (old, ill, or
depressed people); people with particular diseases or medical problems; people dealing with
complex cognitive tasks, such as reading acquisition; people who are blind or who have hearing
impairment; fetuses, babies and young children; and the elderly in general (Jansen 1987; AAP
1997). These people may be less able to cope with the impacts of noise exposure and be at
greater risk for harmful effects.
Persons with impaired hearing are the most adversely affected with respect to speech
intelligibility. Even slight hearing impairments in the high-frequency range may cause problems
with speech perception in a noisy environment. From about 40 years of age, people typically
demonstrate an impaired ability to understand difficult, spoken messages with low linguistic
redundancy. Therefore, based on interference with speech perception, a majority of the
population belongs to the vulnerable group.
Children have also been identified as vulnerable to noise exposure (see Agenda 21: UNCED
1992). The evidence on noise pollution and childrens health is strong enough to warrant
monitoring programmes at schools and preschools to protect children from the effects of noise.
Follow up programmes to study the main health effects of noise on children, including effects on
speech perception and reading acquisition, are also warranted in heavily noise polluted areas
(Cohen et al. 1986; Evans et al. 1998).

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The issue of vulnerable subgroups in the general population should thus be considered when
developing regulations or recommendations for the management of community noise. This
consideration should take into account the types of effects (communication, recreation,
annoyance, etc.), specific environments (in utero, incubator, home, school, workplace, public
institutions, etc.) and specific lifestyles (listening to loud music through headphones, or at
discotheques and festivals; motor cycling, etc.).

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